Ann Thorac Surg 2000;69:1266-1268
© 2000 The Society of Thoracic Surgeons
CASE REPORTS
Massive cerebral embolization: successful treatment with retrograde perfusion
John A. Kern, MDa,
Scott Arnold, MDa
a Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Virginia Health Sciences Center, Charlottesville, Virginia, USA
Address reprint requests to Dr Kern, Department of Surgery, University of Virginia Health Sciences Center, Box 310-88, Charlottesville, VA 22908
e-mail: jak3r{at}virginia.edu
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Abstract
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Stroke is an unpredictable and morbid complication of cardiac operations. We report a patient who suffered massive bilateral cerebral embolization during aortic cannulation for coronary bypass. This was treated successfully with hypothermic circulatory arrest and high flow retrograde cerebral perfusion. The patient suffered only minimal neurologic impairment and improved rapidly. She was discharged home on postoperative day 7 neurologically intact.
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Introduction
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Stroke and neurologic dysfunction are unpredictable and devastating complications of cardiac operations. Although the cause of postoperative neurologic impairment varies, particulate embolization as a result of aortic manipulation is most common [1]. While there are many markers of a potentially "bad" aorta, occasionally a normal-appearing aorta in a low-risk patient will harbor deadly atheromatous debris. Through the use of intraoperative epiaortic ultrasound, intraluminal atheroma often can be detected and measures taken to minimize the risk of embolic stroke [2]. In addition, with the advent of "off-pump" cardiac operations many patients with diseased aortas can undergo surgical procedures without the use of cardiopulmonary bypass, reducing the risk of stroke even further. If cardiopulmonary bypass is required, however, and if the aortic cannula fills with atheromatous debris that had gone undiagnosed previously, the patient’s fate is usually sealed. We describe a patient who suffered extensive cerebral particulate embolization at the time of aortic cannulation, whom we salvaged through the use of hypothermic circulatory arrest and high flow retrograde cerebral perfusion.
A 73-year-old noninsulin-dependent diabetic woman with a history of extracranial cerebral vascular disease (s/p right carotid endarterectomy), chronic obstructive pulmonary disease, and smoking was referred for coronary revascularization because of angina and dyspnea on exertion. Cardiac catheterization revealed critical left main and circumflex disease with no evidence of ostial stenosis, and her aorta was free of calcification. Her renal function was normal and she had no evidence of recurrent carotid stenosis. Aortic calcification was not present on her chest radiograph. At operation her aorta was gently palpated, was free of calcific plaques, and by external appearance looked normal. When the aortic cannula was inserted a large piece of atheromatous debris 3 cm long completely filled the lumen of the cannula. The cannula was burped until all debris was flushed from the cannula and blood return was normal. The patient was rapidly placed on cardiopulmonary bypass while holding pressure over the carotid arteries and she was cooled to 18°C. While cooling, antegrade and retrograde cardioplegic delivery systems were established and a separate coronary sinus catheter was placed in the superior vena cava (SVC) for retrograde cerebral perfusion. Blood pressure cuffs were placed on each arm. After the patient was cooled, the blood pressure cuffs were inflated and cardiopulmonary bypass was discontinued. Retrograde cerebral perfusion (cold blood at 12°C) was begun through the SVC cannula while the ascending aorta was opened transversely proximal to the aortic cannula. The inferior vena cava was not snared or pressurized. Antegrade cardioplegia was given followed by continuous retrograde cardioplegia. A large atheromatous deposit was present on the distal ascending aorta and proximal lesser curve of the arch, just opposite the origin of the innominate artery. The plaque was located such that the aortic cannula traversed a large mass of loose atheroma during insertion. The remainder of the aorta was normal. Retrograde SVC flow was increased to 800 cc/min, which produced a pressure of 45 mm Hg in the SVC. Particulate debris was seen coming out of the innominate and left carotid arteries. The atheromatous plaque was debrided and retrograde SVC perfusion was continued for 30 minutes. The aortotomy was closed, air was removed from the aorta, and cardiopulmonary bypass was reinstituted. The operation was completed without any further difficulty and she weaned easily from bypass.
She awoke neurologically intact. After extubation, a detailed neurologic examination revealed minor difficulties with fine motor function, short-term memory, and her ability to follow complex commands. A magnetic resonance image revealed multiple bilateral cerebral and cerebellar embolic infarcts (Fig 1). Her neurologic function improved to baseline by 1 week and she was discharged home. No other immediate signs of systemic embolization were evident. Her extremities were normal, her renal function did not immediately suffer, and her gastrointestinal tract functioned normally.
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Fig 1. Magnetic resonance images from postoperative day 3 showing evidence of multiple bilateral cerebral (A) and cerebellar (B) infarcts.
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Six weeks after operation she developed worsening renal function. Ultimately, a renal biopsy was done which revealed evidence of cholesterol embolization. Unfortunately her renal function deteriorated and she is now dialysis dependent. Her neurologic function remains normal.
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Comment
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Stroke is a devastating and unpredictable complication of cardiac operations and significant neurologic deficits occur in 1% to 5% of patients undergoing cardiac surgical procedures [3, 4]. There are several causes for the development of neurologic deficits and the most common are embolic phenomena. Patients with atherosclerotic ascending aortas are at the greatest risk for embolic strokes unless the disease is recognized and operative strategy is modified. Advanced age, diabetes, extracranial carotid disease, and aortic calcification on chest radiograph are all markers of a potentially "bad" aorta [1–3]. Intraoperative epiaortic ultrasound has proved useful for screening high-risk patients. When significant atheromatous debris is seen, operative technique can be modified to avoid or remove the offending plaque. Although our patient had risk factors for aortic disease, she had no aortic calcification and epiaortic ultrasound was not done.
After cardiac operation the degree of neurologic impairment has been correlated to the number of embolic particles. Studies have documented worsening neurologic outcome with increasing number of emboli. Transcranial imaging studies also have documented that cerebral emboli are most likely to occur during aortic cannulation or placement of the aortic cross clamp [5]. If significant aortic atheromatous debris goes unrecognized, cannulation can be a terminal event.
Retrograde cerebral perfusion (RCP) is a technique first described in 1980 as a means of treating massive air embolism [6]. As experience grew, reports appeared documenting the benefits of RCP on neurologic outcome, possibly through cerebral nutrient and oxygen supply, during extended periods of hypothermic circulatory arrest (HCA) during difficult aortic arch reconstructions. In addition, many surgeons believe that with retrograde flow the chance of particulate debris embolizing to the brain is reduced. Few data exist, however, supporting the effectiveness of RCP for the treatment of known cerebral emboli.
Two experimental studies from Griepp’s group at Mount Sinai Medical Center in New York have examined the benefit of RCP in treating cerebral particulate embolization in a porcine model [7, 8]. Their results show that RCP may be effective in removing particulate emboli from the brain and also may mitigate the severity of cerebral injury. However, potential for harm through uncontrolled perfusion pressure may be a limiting factor for this technique. In clinical practice, most surgeons use RCP electively during aortic reconstructions requiring circulatory arrest, and SVC pressures are generally maintained less than 30 to 35 mm Hg. Clinical guidelines for the use of RCP in treating particulate cerebral emboli are not established. It is our belief that higher pressures and flow rates may be in order for adequate treatment of particulate embolization.
Because we were able to clear the cannula of atheromatous debris, we used the aortic cannula that was in place to rapidly institute cardiopulmonary bypass. We cooled to a temperature of 18°C. We believe that cooling may have limited the extent of the infarcts by protecting the peri-infarct zone until adequate nutrient flow could be reestablished. In addition, to direct more flow to the brain we placed a blood pressure cuff on each arm. Although most protocols for RCP include SVC flow rates of 350 to 500 cc/min and SVC pressures of 30 to 35 mm Hg, we believed we had little to lose by raising these limits. We ultimately achieved a flow of 800 cc/min and a SVC pressure of 45 mm Hg. With this degree of perfusion, we saw clear evidence of particulate debris being flushed from the head vessels. The 30-minute period of retrograde perfusion was arbitrary and we believed that beyond this time additional benefit was unlikely. This technique did not completely abrogate the embolic burden (as documented by magnetic resonance imaging), but we believe the extent of neurologic impairment was minimized. Although speculative, we believe the ischemic peri-infarct zones were resuscitated during the period of cold retrograde perfusion while the embolic particles were flushed out.
We believe that retrograde SVC perfusion should be considered a potential treatment for any patient who suffers cerebral particulate emboli during cardiac operation. The standard practice of low perfusion pressure during "routine retrograde cerebral perfusion" may not be adequate in these extreme cases of particulate embolization.
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References
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Accepted for publication September 9, 1999.
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Abstract
Introduction
